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Diaphragm dysfunction in chronic obstructive pulmonary disease.

Coen A C Ottenheijm¹, Leo M A Heunks, Gary C Sieck

¹Department of Pulmonary Diseases, Radboud University Nijmegen Medical Centre, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands.

American Journal of Respiratory and Critical Care Medicine

|April 26, 2005

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Diaphragm muscle fibers in chronic obstructive pulmonary disease (COPD) patients show reduced force and myosin content. Enhanced protein degradation via the ubiquitin-proteasome pathway contributes to this diaphragm weakness in COPD.

Area of Science:

Respiratory Physiology
Muscle Biology
Biochemistry

Background:

Hypercapnic respiratory failure due to inspiratory muscle weakness is a major cause of mortality in chronic obstructive pulmonary disease (COPD).
The precise mechanisms underlying diaphragm muscle force generation failure in COPD remain incompletely understood.

Purpose of the Study:

To investigate the contractile function and myosin heavy chain content of diaphragm muscle single fibers in patients with COPD.
To explore the role of protein degradation pathways in diaphragm dysfunction in COPD.

Main Methods:

Single skinned muscle fibers were isolated from diaphragm biopsies of COPD patients and controls.
Contractile function, myosin heavy chain content, and Ca2+ sensitivity were assessed in individual fibers.

Related Experiment Videos

Ubiquitin-protein conjugation levels were measured in diaphragm muscle homogenates.

Main Results:

Diaphragm fibers from COPD patients exhibited reduced force generation per cross-sectional area and lower myosin heavy chain content.
Impaired Ca2+ sensitivity and slower cross-bridge cycling kinetics were observed in COPD diaphragm fibers.
Increased ubiquitin-protein conjugation was detected in diaphragm muscle homogenates from COPD patients.

Conclusions:

Diaphragm fiber contractile function is impaired early in the progression of COPD.
Enhanced protein degradation via the ubiquitin-proteasome pathway likely contributes to the loss of contractile proteins and subsequent diaphragm force failure in COPD.